Facts about Iodine and Autoimmune Thyroiditis - Beck Natural ...

Facts about Iodine and Autoimmune Thyroiditis
by Guy E. Abraham, MD
Since the 2006 publication by Tang, et al, 1 reporting a positive association between iodization of
salt in China and autoimmune thyroiditis (AIT), I have received a lot of calls and e-mails
questioning the use of iodine in patients with autoimmune thyroiditis. Iodophobes were elated
with this publication, which vindicated their iodophobic viewpoint. However, a year later in
2007, the same authors, using the same data 2 retracted their original statement and concluded
that: “Chronic iodine excess does not apparently increase the risk of autoimmune thyroiditis.”
I will present some facts about iodine and autoimmune thyroiditis.
In 1912, pathologist H. Hashimoto published in a German medical journal, 3 his histological
findings in four thyroid glands removed at surgery: numerous lymphoid follicles; extensive
connective tissue formation; diffuse round cell infiltration; and significant changes of the acinar
epithelium. He called this pathology of the thyroid “struma lymphomatosa”, but it became
popular under the name “Hashimoto thyroiditis”. At the time of Hashimoto’s publication,
autoimmune thyroiditis was not observed in the US population until the iodization of salt.
Hashimoto’s thyroiditis is now classified as goitrous AIT because the gland is enlarged, in
distinction to atrophic AIT where atrophy and fibrosis are predominant. Both conditions are
chronic, progressing over time to hypothyroidism in a significant percentage of patients. 4
In several communities worldwide, an increased incidence of AIT was reported following
implementation of iodization of sodium chloride. 5 In areas of the US where this relationship has
been studied, mainly in the Great Lakes Region, a similar trend was reported. In 1966 and 1968,
Weaver, et al, 6,7 from Ann Arbor, Michigan reported: “The salient histopathological feature of
the thyroid glands, removed at operation in a five-year period before iodine prophylaxis (1915-
1920), was the paucity of lymphocytes in their parenchyma and, more importantly, the absence
of thyroiditis of any form … It should be emphasized that the thyroid glands prior to the use of
iodized salt were devoid of lymphocytes, and nodular colloid goiters with dense lymphocytic
infiltrates were found after the introduction of iodized salt in 1924.”

Furszyfer, et al, 8 from the Mayo Clinic, studied the average annual incidence of Hashimoto’s
thyroiditis among women of Olmsted County, Minnesota, during three consecutive periods
covering 33 years of observation, from 1935 to 1967. They found the incidence to be higher in
women 40 years and older versus women 39 years and younger. However, in both groups, there
was a progressive increase in the incidence of Hashimoto’s thyroiditis over time. During the
three periods evaluated — 1935-1944; 1945-1954; 1955-1967 — the average annual incidence of
Hashimoto’s per 100,000 population were 2.1, 17.9, and 54.1 for women 39 years and less. For
women 40 years and older, the average annual incidence over the same three periods were 16.4,
27.4, and 94.1.
It is important to point out that the Mayo Clinic study started 10-15 years after implementation of
iodization of salt in the area. Therefore, even during the first decade of observation, the
prevalence of AIT was already significant. Again, it must be emphasized that prior to the
implementation of iodized salt as observed by Weaver, et al, 6,7 this pathology of the thyroid
gland was not reported in the US, even though Lugol solution and potassium iodide were used
extensively in medical practice at that time in daily amounts two orders of magnitude greater
than the average intake of iodide from table salt. 4 This suggests that inadequate iodide intake
aggravated by goitrogens, not excess iodide, was the cause of this condition. To be discussed
later, AIT cannot be induced by inorganic iodide in laboratory animals unless combined with
goitrogens, therefore inducing iodine deficiency.
The pathophysiology of AIT is poorly understood. Experimentally induced autoimmune
thyroiditis in laboratory animals by acutely administered iodide required the use of antithyroid
drugs, essentially goitrogens, to produce these effects. 9-12 These goitrogens induced thyroid
hyperplasia and iodide deficiency. Antioxidants either reduced or prevented the acute iodideinduced
thyroiditis in chicks 13 and mice. 14 Bagchi, et al, 13 and Many, et al, 14 proposed that the
thyroid injury induced by the combined use of iodide and goitrogens occurs through the
generation of reactive oxygen species.
We have previously proposed a mechanism for the oxidative damage caused by low levels of
iodide combined. with antithyroid drugs: 2 Inadequate iodide supply to the thyroid gland,
aggravated by goitrogens, activates the thyroid peroxydase (TPO) system through elevated TSH,
low levels of iodinated lipids, and high cytosolic free calcium, resulting in excess production of
H 2 O 2 . The excess H 2 O 2 production is evidenced by the fact that antioxidants used in Bagchi’s
experiments did not interfere with the oxidation and organification of iodide and therefore
neutralized only the excess oxidant. 11 This H 2 O 2 production is above normal due to a deficient
feedback system, caused by high cytosolic calcium due to magnesium deficiency and low levels
of iodinated lipids which requires for their synthesis iodide levels two orders of magnitude
greater than the RDA for iodine. 4 Once the low iodide supply is depleted, TPO in the presence of
H 2 O 2 and organic substrate reverts to its peroxydase function, which is the primary function of

haloperoxydases, causing oxidative damage to molecules nearest to the site of action: TPO and
the substrate thyroglobulin (Tg). Oxidized TPO and Tg elicit an autoimmune reaction with
production of antibodies against these altered proteins with subsequent damage to the apical
membrane of the thyroid cells, resulting in the lymphocytic infiltration and in the clinical
manifestations of Hashimoto’s thyroiditis. Eventually, the oxidative damage to the TPO results
in deficient H 2 O 2 production. Hypothyroidism occurs in AIT when oxidation and organification
of iodide in the thyroid gland become deficient enough to affect synthesis of thyroid hormones.
In vitro studies with purified fractions of calf thyroid glands by De Groot, et al, 15 gave
compelling evidence that iodide at 10-5 molar confers protection to TPO against oxidative
damage. To achieve peripheral levels of 10-5 molar iodide, a human adult needs a daily amount
of 50-100 mg. DeGroot’s findings can be summarized as follows:
• TPO is inactivated by H 2 O 2 .
• KI at 10-5 molar protects TPO from oxidative damage.
• Potassium bromide and potassium fluoride do not share this protective effect of KI.
• The protective effect of KI is not due to the covalent binding of iodine to TPO but due to the
presence of KI itself in the incubation media.
The concentrations of iodine measured in the thyroid of patients with AIT are the lowest
observed. Further, AIT patients with hypothyroidism have significantly lower iodine levels in the
thyroid gland than AIT patients with normal thyroid function. For the US population, Okerlund 16
reported a mean value of around 10 mg iodine/ thyroid, with a range of 4-19 mg. In 56 patients
suffering from autoimmune thyroiditis, but with normal thyroid function, a mean value of 4.8
mg/thyroid was reported. In 13 patients with autoimmune thyroiditis and hypothyroidism, the
mean value was 2.3 mg/thyroid.
Based on the above facts, it is obvious that iodine deficiency, not excess, is the cause of AIT.
REFERENCES

1) Teng, et al. “Effect of iodine intake on thyroid disease in China.” New England Medical
Journal, 2006; 354:2783-93.
2) Yang F, et al. “Chronic iodine does not increase the incidence of hyperthyroidism: A
prospective community-based epidemiological survey in China.” Eur J Endocrinol, 2007;
156(4):403-8.
3) Hashimoto H. “Zur Kenntniss der lymphomatosen Veranderung der Schilddruse (Struma
lymphomatosa).” Arch Klin Chir, 1912; 97:219-248.
4) Abraham GE. “The safe and effective implementation of orthoiodosupplementation in medical
practice.” The Original Internist, 2004; 11(1):17-36.
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J Surg, 1991; 15:205-215.
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goiters.’” Arch Surg, 1968; 98:183-186.
7) Weaver DK, Nishiyama RH, et al. “Surgical thyroid disease.” Arch Surg, 1966; 92:796-801.
8) Furszyfer J, Kurland LT, et al. “Hashimoto’s thyroiditis in Olmsted County, Minnesota, 1935
through 1967.” Mayo Clin Proc, 1970; 45:586-596.
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13) Bagchi N, Brown TR, and Sundick RS. “Thyroid cell injury is an initial event in the
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14) Many MC, Papadopoulaous J, et al. “Iodine-induced cell damage in mouse hyperplastic
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and Hennenian G, editors. Proceedings of the 10th International Thyroid Conference. Balkema,
Rotterdam, 1991; 635-638.
15) DeGroot Leslie J, et al. “Studies on an iodinating enzyme from calf thyroid.” Endocrinology,
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